,[19] Tenovero et al.,[23] Harrison et al.,[24] Pal et al.,[25] and L��pez et al.[26] The increased salivary total protein in diabetics could be attributed to the increase in basement membrane permeability, allowing easy and increased passage of serum proteins into the whole saliva via salivary gland and gingival crevices.[23,27,28] http://www.selleckchem.com/products/Gemcitabine-Hydrochloride(Gemzar).html Arati et al. and Streckfus et al. have demonstrated highly significant positive correlations in salivary total protein levels among uncontrolled and controlled diabetic groups.[11,19,21] CONCLUSION Diabetes mellitus is known to alter the composition of saliva. A few reported studies have shown alteration of salivary constituents in diabetes mellitus.
Hence, the purpose of this study was to estimate and compare the levels of salivary potassium, sodium, and total protein in smoker diabetic patients and nondiabetic smokers and controls, and to explore potential of salivary electrolytes [Na+, K+] and total proteins as markers. The estimated values of salivary constituents add to the data already recorded in Indian population. However, further studies using large samples are required to evaluate the findings in our study. Footnotes Source of Support: Nil Conflict of Interest: None declared.
Hypertensive disorders such as chronic hypertension, gestational hypertension, and pre-eclampsia (PE) complicate approximately 5-7% of all pregnancies,[1] with PE being dominant, affecting 3-5% of pregnancies.[2] The diagnosis of PE is made based on the presence of both hypertension and proteinuria after 20 weeks of gestation.
Changes that are observed in PE are usually pregnancy-induced and regress after delivery.[3] The symptoms of PE not only reflect damage to the uterus, fetus, and placenta, but to the kidneys as well.[4] Though PE is of unknown etiology, there are risk factors that are associated with the disorder, such as gestational and type 1 diabetes mellitus, obesity, and chronic hypertension.[5] It has been reported that PE originates in the placenta.[6] Placental vascular abnormalities associated with PE contribute to fetal intrauterine Anacetrapib growth restriction (IUGR). PE is among the leading causes of IUGR and results from the impairment of materno-fetal exchanges. These impairments in materno-fetal exchanges coincide with the onset of PE in the third trimester of pregnancy.[7] Nitric oxide (NO), which is generated by the endothelial cells, has been implicated in the pathogenesis of PE. Its production plays an integral role in homeostatic vasodilation and is believed to contribute to the vasodilation of normal pregnancy.[8] The biosynthesis of NO and cGMP increases during pregnancy in rats.